ArticleHuman mutation2017
Understanding the Genomic Structure of Copy-Number Variation of the Low-Affinity Fcγ Receptor Region Allows Confirmation of the Association of FCGR3B Deletion with Rheumatoid Arthritis.
Article in Human mutation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Association of Fc Gamma Receptor 3B Gene Copy Number Variation with Rheumatoid Arthritis Susceptibility.Genes · 2022Pooled it
- Complete CD16A Deficiency and Defective NK Cell Function in a Man Living with HIV.Journal of clinical immunology · 2025Article
- Structural polymorphism and diversity of human segmental duplications.Nature genetics · 2025Article
- Identification of novel drug targets through integrative PWAS of brain and plasma proteins with Ulcerative Colitis GWAS.PloS one · 2025Article
- Pitfalls When Determining HNA-1 Genotypes and Finding Novel Alleles.International journal of molecular sciences · 2024Article
- Protein-altering variants at copy number-variable regions influence diverse human phenotypes.Nature genetics · 2024Article
- Article
- An Update Evolving View of Copy Number Variations in Autoimmune Diseases.Frontiers in genetics · 2021Review
- Identification of Common Differentially Expressed Genes and Potential Therapeutic Targets in Ulcerative Colitis and Rheumatoid Arthritis.Frontiers in genetics · 2020Article
- Genetic Variation in Low-To-Medium-Affinity Fcγ Receptors: Functional Consequences, Disease Associations, and Opportunities for Personalized Medicine.Frontiers in immunology · 2019Review
- Article
- Copy Number Variation Disorders.Current genetic medicine reports · 2017Article
- Population genetics of immune-related multilocus copy number variation in Native Americans.Journal of the Royal Society, Interface · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Fcγ receptors are a family of cell-surface receptors that are expressed by a host of different innate and adaptive immune cells, and mediate inflammatory responses by binding the Fc portion of immunoglobulin G. In humans, five low-affinity receptors are encoded by the genes FCGR2A, FCGR2B, FCGR2C, FCGR3A, and FCGR3B, which are located in an 82.5-kb segmental tandem duplication on chromosome 1q23.3, which shows extensive copy-number variation (CNV). Deletions of FCGR3B have been suggested to increase the risk of inflammatory diseases such as systemic lupus erythematosus and rheumatoid arthritis (RA). In this study, we identify the deletion breakpoints of FCGR3B deletion alleles in the UK population and endogamous native American population, and show that some but not all alleles are likely to be identical-by-descent. We also localize a duplication breakpoint, confirming that the mechanism of CNV generation is nonallelic homologous recombination, and identify several alleles with gene conversion events using fosmid sequencing data. We use information on the structure of the deletion alleles to distinguish FCGR3B deletions from FCGR3A deletions in whole-genome array comparative genomic hybridization (aCGH) data. Reanalysis of published aCGH data using this approach supports association of FCGR3B deletion with increased risk of RA in a large cohort of 1,982 cases and 3,271 controls (odds ratio 1.61, P = 2.9×10
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